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Vol. 13. Núm. 2.
Páginas 111-121 (junio 2009)
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Vol. 13. Núm. 2.
Páginas 111-121 (junio 2009)
Open Access
Factores que influyen en el curso de la infección por el virus de la inmunodeficiencia humana tipo 1 en individuos sin progresión a largo plazo
Factors influencing the course of type one human immunodeficiency virus infection in individuals classified as long term non-progressors
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1980
Juan Camilo Patiño1, Paula Andrea Velilla1, María Teresa Rugeles1,
Autor para correspondencia
mtrugel@udea.edu.co

Correspondencia: Calle 62 N° 52-59, Laboratorio 532, SIU, Medellín, Colombia.
1 Grupo de Inmunovirología, Sede de Investigación Universitaria, Universidad de Antioquia, Medellín, Colombia
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Resumen

La historia natural de la infección por el virus de la inmunodeficiencia humana tipo 1 (VIH-1) es un proceso variable que ha permitido identificar individuos con diferentes patrones de progresión de la infección. Entre estos individuos, existe un grupo de personas catalogadas como, sin progresión a largo plazo, las cuales se caracterizan por permanecer asintomáticas por largos periodos, sin evidencia de deterioro inmunológico y con cargas virales bajas o indetectables, en ausencia de tratamiento antirretroviral. Diferentes factores inmunológicos, genéticos y virales se han asociado con el patrón de progresión exhibido por estos individuos. Los factores inmunológicos contemplan mecanismos tanto de la inmunidad innata como de la adaptativa; los factores genéticos están relacionados con los genes que codifican los receptores de quimiocinas y sus ligandos naturales y genes del complejo mayor de histocompatibilidad. Por otro lado, los factores virales están relacionados con la variabilidad genética del virus y con su capacidad de replicación.

De la forma en que estos factores se interrelacionen, dependen la capacidad infecciosa del virus, la respuesta inmune anti-VIH que pueda establecer el hospedero y, por consiguiente, el patrón de progresión que se establezca.

Palabras clave:
VIH-1
progresión a largo plazo
resistencia natural
Summary

The natural history of type one human immunodeficiency virus infection (HIV-1) is a variable process that has allowed identifying different patterns of progression. Among them, there is a group of individuals known as long-term non-progressors (LTNP). LTNP are characterized for being asymptomatic for long periods of time, showing no evidence of immune deterioration and having low or undetectable viral loads in absence of antiretroviral treatment. Different immunologic, genetic and viral factors have been associated with the pattern of progression. Immunological factors include both, innate and adaptive mechanisms; genetic factors are related with genes of the chemokines family as well as genes of the major histocompatibility complex. On the other hand, viral factors are related to the genetic variability and replication ability of the virus. The disease pattern that is established depends on the interrelations of all these factors, which finally account for the type of anti- HIV-1 immune response developed and the infectious capacity of the virus.

Key words:
HIV-1
long-term non-progressors
natural resistance
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Referencias
[1.]
V. Soriano, R. Martin, J. Del Romero, et al.
Rapid and slow progression of the infection by the type 1 human immunodeficiency virus in a population of seropositive subjects in Madrid.
Med Clin (Barc), 107 (1996), pp. 761-766
[2.]
L.E. Soto.
Mecanismos patogénicos de la infección por VIH.
Rev Invest Clin, 56 (2004), pp. 143-152
[3.]
P.J. Easterbrook.
Non-progression in HIV infection.
AIDS, 8 (1994), pp. 1179-1182
[4.]
J.A. Levy.
HIV pathogenesis and long-term survival.
AIDS, 7 (1993), pp. 1401-1410
[5.]
Y. Cao, L. Qin, L. Zhang, J. Safrit, D.D. Ho.
Virologic and immunologic characterization of long-term survivors of human immunodeficiency virus type 1 infection.
New Engl J Med, 332 (1995), pp. 201-208
[6.]
G. Pantaleo, A.S. Fauci.
New concepts in the immunopathogenesis of HIV infection.
Annu Rev Immunol, 13 (1995), pp. 487-512
[7.]
A. Oliva, A.L. Kinter, M. Vaccarezza, A. Rubbert, A. Catanzaro, S. Moir.
Natural killer cells from human immunodeficiency virus (HIV) -infected individuals are an important source of CC-chemokines and suppress HIV-1 entry and replication in vitro.
J Clin Invest, 102 (1998), pp. 223-231
[8.]
V. Soumelis, I. Scott, F. Gheyas, D. Bouhour, G. Cozon, L. Cotte, et al.
Depletion of circulating natural type 1 interferon- producing cells in HIV-infected AIDS patients.
Blood, 98 (2001), pp. 906-912
[9.]
J. Stebbing, B. Gazzard, L. Kim, S. Portsmouth, A. Wildfire, I. Teo, et al.
The heat-shock protein receptor CD91 is upregulated in monocytes of HIV-1-infected “true” long-term nonprogressors.
Blood, 101 (2003), pp. 4000-4004
[10.]
H. Ullum, A. Cozzi Lepri, J. Victor, H. Aladdin, A.N. Phillips, J. Gerstoft, et al.
Production of beta-chemokines in human immunodeficiency virus (HIV) infection: evidence that high levels of macrophage inflammatory protein-1beta are associated with a decreased risk of HIV disease progression.
J Infect Dis, 177 (1998), pp. 331-336
[11.]
Q. Li, L. Duan, Estes Jd, Z.M. Ma, T. Rourke, Y. Wang, et al.
Peak SIV replication in resting memory CD4+ T cells depletes gut lamina propria CD4+ T cells.
Nature, 434 (2005), pp. 1148-1152
[12.]
E. Barker, C.E. Mackewicz, G. Reyes-Teran, A. Sato, S.A. Stranford, S.H. Fujimura, et al.
Virological and immunological features of long-term human immunodeficiency virus-infected individuals who have remained asymptomatic compared with those who have progressed to acquired immunodeficiency syndrome.
Blood, 92 (1998), pp. 3105-3114
[13.]
E.S. Rosenberg, J.M. Billingsley, A.M. Caliendo, S.L. Boswell, P.E. Sax, S.A. Kalams, et al.
Vigorous HIV-1-specific CD4+ T cell responses associated with control of viremia.
Science, 278 (1997), pp. 1447-1450
[14.]
N. Imami, A. Pires, G. Hardy, J. Wilson, B. Gazzard, F. Gotch.
A balanced type 1/type 2 response is associated with longterm nonprogressive human immunodeficiency virus type 1 infection.
J Virol, 76 (2002), pp. 9011-9023
[15.]
X. Jin, D.E. Bauer, S.E. Tuttleton, S. Lewin, A. Gettie, J. Blanchard, et al.
Dramatic rise in plasma viremia after CD8(+) T cell depletion in simian immunodeficiency virus-infected macaques.
JEM, 189 (1999), pp. 991-998
[16.]
J. Nilsson, A. Boasso, P.A. Velilla, R. Zhang, M. Vaccari, G. Franchini, et al.
HIV-1-driven regulatory T-cell accumulation in lymphoid tissues is associated with disease progression in HIV/AIDS.
Blood, 108 (2006), pp. 3808-3817
[17.]
M. Paroli, A. Propato, D. Accapezzato, V. Francavilla, E. Schiaffella, V. Barnaba.
The immunology of HIV-infected long-term non-progressors -a current view.
Immunol Lett, 79 (2001), pp. 127-129
[18.]
M.R. Betts, J.F. Krowka, T.B. Kepler, M. Davidian, C. Christopherson, S. Kwok, et al.
Human immunodeficiency virus type 1-specific cytotoxic T lymphocyte activity is inversely correlated with HIV type 1 viral load in HIV type 1-infected long-term survivors.
AIDS Res Hum Retroviruses, 15 (1999), pp. 1219-1228
[19.]
D.J. Blackbourn, C.E. Mackewicz, E. Barker, T.K. Hunt, B. Herndier, A.T. Haase, et al.
Suppression of HIV replication by lymphoid tissue CD8+ cells correlates with the clinical state of HIV-infected individuals.
PNAS, 93 (1996), pp. 13125-13130
[20.]
C.E. Mackewicz, H.W. Ortega, J.A. Levy.
CD8+ cell anti-HIV activity correlates with the clinical state of the infected individual.
J Clin Invest, 87 (1991), pp. 1462-1466
[21.]
C.E. Mackewicz, L.C. Yang, J.D. Lifson, J.A. Levy.
Non-cytolytic CD8 T-cell anti-HIV responses in primary HIV-1 infection.
Lancet, 344 (1994), pp. 1671-1673
[22.]
W. Zapata, C.J. Montoya, M.T. Rugeles.
Soluble factors with inhibitory activity against type 1 human immunodeficiency virus.
Biomédica, 26 (2006), pp. 451-466
[23.]
R. Kamin-Lewis, S.F. Abdelwahab, C. Trang, A. Baker, A.L. DeVico, R.C. Gallo, et al.
Perforing-low memory CD8+ cells are the predominant T cells in normal humans that synthesize the beta -chemokine macrophage inflammatory protein-1beta.
PNAS, 98 (2001), pp. 9283-9288
[24.]
D.C. Montefiori, G. Pantaleo, L.M. Fink, J.T. Zhou, J.Y. Zhou, M. Bilska, et al.
Neutralizing and infection-enhancing antibody responses to human immunodeficiency virus type 1 in longterm nonprogressors.
J Infect Dis, 173 (1996), pp. 60-67
[25.]
S. Rusconi, A. Berlusconi, L. Papagno, M.C. Colombo, C. De Maddalena, A. Riva, et al.
Patterns of in vitro anti-human immunodeficiency virus type 1 antibody production in long-term nonprogressors.
Clin Immunol Immunopathol, 85 (1997), pp. 320-323
[26.]
M.W. Richardson, J. Mirchandani, J. Duong, S. Grimaldo, V. Kocieda, H. Hendel, et al.
Antibodies to Tat and Vpr in the GRIV cohort: differential association with maintenance of long-term non-progression status in HIV-1 infection.
Biomed Pharmacother, 57 (2003), pp. 4-14
[27.]
L. Furci, G. Scarlatti, S. Burastero, et al.
Antigen-driven C-C chemokine-mediated HIV-1 suppression by CD4(+) T cells from exposed uninfected individuals expressing the wild-type CCR-5 allele.
JME, 186 (1997), pp. 455-460
[28.]
M. Dean, M. Carrington, C. Winkler, G.A. Huttley, M.W. Smith, R. Allikmets, et al.
Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Hemophilia Growth and Development Study, Multicenter AIDS Cohort Study, Multicenter Hemophilia Cohort Study, San Francisco City Cohort, ALIVE Study.
Science, 273 (1996), pp. 1856-1862
[29.]
J. Reynes, P. Portales, M. Segondy, V. Baillat, P. André, B. Réant, et al.
CD4+ T cell surface CCR5 density as a determining factor of virus load in persons infected with human immunodeficiency virus type 1.
J Infect Dis, 181 (2000), pp. 927-932
[30.]
M.P. Martin, M. Dean, M.W. Smith, C. Winkler, B. Gerrard, N.L. Michael, et al.
Genetic acceleration of AIDS progression by a promoter variant of CCR5.
Science, 282 (1998), pp. 1907-1911
[31.]
A.O. Clegg, L.J. Ashton, R.A. Biti, P. Badhwar, P. Williamson, J.M. Kaldor, et al.
CCR5 promoter polymorphisms, CCR5 59029A and CCR5 59353C, are under represented in HIV- 1-infected long-term non-progressors. The Australian Long- Term Non-Progressor Study Group.
AIDS, 14 (2000), pp. 103-108
[32.]
L.G. Kostrikis, Y. Huang, J.P. Moore, S.M. Wolinsky, L. Zhang, Y. Guo, et al.
A chemokine receptor CCR2 allele delays HIV-1 disease progression and is associated with a CCR5 promoter mutation.
Nat Med, 4 (1998), pp. 350-353
[33.]
F. Vidal, C. Vilades, P. Domingo, M. Broch, E. Pedrol, D. Dalmau, et al.
Spanish HIV-1-infected long-term nonprogressors of more than 15 years have an increased frequency of the CX3CR1 249I variant allele.
J Acquir Immune Defic Syndr, 40 (2005), pp. 527-531
[34.]
A. Aiuti, I.J. Webb, C. BleuL., T. Springer, J.C. Gutierrez-Ramos.
The chemokine SDF-1 is a chemoattractant for human CD34+ hematopoietic progenitor cells and provides a new mechanism to explain the mobilization of CD34+ progenitors to peripheral blood.
JEM, 185 (1997), pp. 111-120
[35.]
C. Winkler, W. Modi, M.W. Smith, G.W. Nelson, X. Wu, M. Carrington, et al.
Genetic restriction of AIDS pathogenesis by an SDF-1 chemokine gene variant. ALIVE Study, Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC).
Science, 279 (1998), pp. 389-393
[36.]
H. Liu, D. Chao, E.E. Nakayama, H. Taguchi, M. Goto, X. Xin, et al.
Polymorphism in RANTES chemokine promoter affects HIV-1 disease progression.
PNAS, 96 (1999), pp. 4581-4585
[37.]
K.S. Macdonald, K.R. Fowke, J. Kimani, V.A. Dunand, N.J. Nagelkerke, T.B. Ball, et al.
Influence of HLA supertypes on susceptibility and resistance to human immunodeficiency virus type 1 infection.
J Infect Dis, 181 (2000), pp. 1581-1589
[38.]
S.J. O’Brien, G.W. Nelson.
Human genes that limit AIDS.
Nat Genet, 36 (2004), pp. 565-574
[39.]
B. Wang, M. Mikhail, W.B. Dyer, J.J. Zaunders, A.D. Kelleher, N.K. Saksena.
First demonstration of a lack of viral sequence evolution in a nonprogressor, defining replication-incompetent HIV-1 infection.
Virology, 312 (2003), pp. 135-150
[40.]
A. Crotti, F. Neri, D. Corti, S. Ghezzi, S. Heltai, A. Baur, et al.
Nef alleles from human immunodeficiency virus type 1-infected long-term-nonprogressor hemophiliacs with or without late disease progression are defective in enhancing virus replication and CD4 down-regulation.
J Virol, 80 (2006), pp. 10663-10674
[41.]
L. Zhang, Y. Huang, H. Yuan, S. Tuttleton, D.D. Ho.
Genetic characterization of vif, vpr, and vpu sequences from longterm survivors of human immunodeficiency virus type 1 infection.
Virology., 228 (1997), pp. 340-349
[42.]
S. Menzo, R. Sampaolesi, E. Vicenzi, E. Santagostino, G. Liuzzi, A. Chirianni, et al.
Rare mutations in a domain crucial for V3-loop structure prevail in replicating HIV from long-term non-progressors.
AIDS, 12 (1998), pp. 985-997
Copyright © 2009. Asociación Colombiana de Infectología (ACIN)
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